Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy - Wikidata - wikimedia - TriplyDB

Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

http://www.wikidata.org/entity/Q35126342

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Bone Marrow Gene Therapy for HIV/AIDS Retroviral integration: Site matters: Mechanisms and consequences of retroviral integration site selection Real-Time Predictions of Reservoir Size and Rebound Time during Antiretroviral Therapy Interruption Trials for HIV Clinical Determinants of HIV-1B Between-Host Evolution and their Association with Drug Resistance in Pediatric Patients Review: Influence of ART on HIV genetics Latency reversal and viral clearance to cure HIV-1.Romidepsin-induced HIV-1 viremia during effective ART contains identical viral sequences with few deleterious mutations.A spatio-temporal assessment of simian/human immunodeficiency virus (SHIV) evolution reveals a highly dynamic process within the host.Dendritic cells restore CD8+ T cell reactivity to autologous HIV-1 HIV-1 antibody 3BNC117 suppresses viral rebound in humans during treatment interruption.HIV latency. Specific HIV integration sites are linked to clonal expansion and persistence of infected cells Large number of rebounding/founder HIV variants emerge from multifocal infection in lymphatic tissues after treatment interruption.Eradicating HIV-1 infection: seeking to clear a persistent pathogen.Determination of HIV-1 coreceptor tropism using proviral DNA in women before and after viral suppression The Tat Inhibitor Didehydro-Cortistatin A Prevents HIV-1 Reactivation from Latency.Longitudinal Analysis of Cerebrospinal Fluid and Plasma HIV-1 Envelope Sequences Isolated From a Single Donor with HIV Asymptomatic Neurocognitive Impairment.Early Antiretroviral Therapy in South African Children Reduces HIV-1-Infected Cells and Cell-Associated HIV-1 RNA in Blood Mononuclear Cells.A new hypothesis on HIV cure.Gene activity in primary T cells infected with HIV89.6: intron retention and induction of genomic repeats.Evaluating Clonal Expansion of HIV-Infected Cells: Optimization of PCR Strategies to Predict Clonality.A Generalized Entropy Measure of Within-Host Viral Diversity for Identifying Recent HIV-1 Infections Early antiretroviral treatment (eART) limits viral diversity over time in a long-term HIV viral suppressed perinatally infected child.Ultrasensitive single-genome sequencing: accurate, targeted, next generation sequencing of HIV-1 RNA.Well-mixed plasma and tissue viral populations in RT-SHIV-infected macaques implies a lack of viral replication in the tissues during antiretroviral therapy.Proviruses with identical sequences comprise a large fraction of the replication-competent HIV reservoir Single Genome Analysis for the Detection of Linked Multiclass Drug Resistance Mutations in HIV-1-Infected Children After Failure of Protease Inhibitor-Based First-Line Therapy.Origin of Rebound Plasma HIV Includes Cells with Identical Proviruses That Are Transcriptionally Active before Stopping of Antiretroviral Therapy.Continued Slow Decay of the Residual Plasma Viremia Level in HIV-1-Infected Adults Receiving Long-term Antiretroviral Therapy.The role of HIV integration in viral persistence: no more whistling past the proviral graveyard.Clonally expanded CD4+ T cells can produce infectious HIV-1 in vivo.Therapeutic Vaccination With Dendritic Cells Loaded With Autologous HIV Type 1-Infected Apoptotic Cells.Envelope gene evolution and HIV-1 neuropathogenesis.Persistent HIV-1 replication maintains the tissue reservoir during therapy Sites of retroviral DNA integration: From basic research to clinical applications What Integration Sites Tell Us about HIV Persistence Host Double Strand Break Repair Generates HIV-1 Strains Resistant to CRISPR/Cas9.HIV-infected cells are frequently clonally expanded after prolonged antiretroviral therapy: implications for HIV persistence.Impact of Depression and Inflammation on the Progression of HIV Disease.Lack of concordance between residual viremia and viral variants driving de novo infection of CD4(+) T cells on ART.Broad activation of latent HIV-1 in vivo.

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Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

http://www.wikidata.org/entity/Q35126342

description

2014 nî lūn-bûn

@nan

2014 թուականի Մարտին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի մարտին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

@zh-hk

2014年論文

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2014年論文

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2014年论文

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name

Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

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Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

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Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

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Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

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Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

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Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

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JOURNAL.PPAT.1004010

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Lack of detectable HIV-1 molecular evolution during suppressive antiretroviral therapy

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Angeline O'Shea

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Carry Poethke

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Catherine Rehm

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Elizabeth M Anderson

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Frank Maldarelli

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John M Coffin

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John W Mellors

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Jonathan Spindler

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Nicholas Kovacs

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Sloane Yu

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P2860

Description and power analysis of two tests for detecting recent population bottlenecks from allele frequency data

Residual human immunodeficiency virus type 1 viremia in some patients on antiretroviral therapy is dominated by a small number of invariant clones rarely found in circulating CD4+ T cells

MEGA5: Molecular Evolutionary Genetics Analysis Using Maximum Likelihood, Evolutionary Distance, and Maximum Parsimony Methods

ART suppresses plasma HIV-1 RNA to a stable set point predicted by pretherapy viremia

The effect of raltegravir intensification on low-level residual viremia in HIV-infected patients on antiretroviral therapy: a randomized controlled trial

HIV population dynamics in vivo: implications for genetic variation, pathogenesis, and therapy

Decay characteristics of HIV-1-infected compartments during combination therapy

Multiple, linked human immunodeficiency virus type 1 drug resistance mutations in treatment-experienced patients are missed by standard genotype analysis.

Multi-site adaptation in the presence of infrequent recombination.

Human immunodeficiency virus replication and genotypic resistance in blood and lymph nodes after a year of potent antiretroviral therapy

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24651464

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antiretroviral drug

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